25iP-NBOMe

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25iP-NBOMe
25iP-NBOMe.svg
Clinical data
ATC code
  • none
Legal status
Legal status
  • DE: NpSG (Industrial and scientific use only)
  • UK: Class A
Identifiers
  • 2-(2,5-Dimethoxy-4-propan-2-ylphenyl)-N-[(2-methoxyphenyl)methyl]ethanamine
CAS Number
PubChem CID
ChemSpider
UNII
Chemical and physical data
Formula C21H29NO3
Molar mass 343.467 g·mol−1
3D model (JSmol)
  • CC(C)C1=C(C=C(C(=C1)OC)CCNCC2=CC=CC=C2OC)OC
  • InChI=1S/C21H29NO3/c1-15(2)18-13-20(24-4)16(12-21(18)25-5)10-11-22-14-17-8-6-7-9-19(17)23-3/h6-9,12-13,15,22H,10-11,14H2,1-5H3
  • Key:KMZZEEDFQLXSQF-UHFFFAOYSA-N

25iP-NBOMe (2C-iP-NBOMe, NBOMe-2C-iP) is a derivative of the phenethylamine hallucinogen 2C-iP, which acts as a highly potent agonist for the human 5-HT2A receptor. [1]

Contents

Toxicity and harm potential

NBOMe compounds are often associated with life-threatening toxicity and death. [2] [3] Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity. [4] Reports of autonomic dysfunction remains prevalent with NBOMe compounds, with most individuals experiencing sympathomimetic toxicity such as vasoconstriction, hypertension and tachycardia in addition to hallucinations. [5] [6] [7] [8] [9] Other symptoms of toxidrome include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death. [5] [9] [3] Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome. [10] The likelihood of seizure is higher in NBOMes compared to other psychedelics. [4]

NBOMe and NBOHs are regularly sold as LSD in blotter papers, [3] [11] which have a bitter taste and different safety profiles. [5] [2] Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity. [2] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD, [7] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently". [5] While most fatalities are due to the physical effects of the drug, there have also been reports of death due to self-harm and suicide under the influence of the substance. [12] [13] [5]

Given limited documentation of NBOMe consumption, the long-term effects of the substance remain unknown. [5] NBOMe compounds are not active orally, [lower-alpha 1] and are usually taken sublingually. [15] :3 When NBOMes are administered sublingually, numbness of the tongue and mouth followed by a metallic chemical taste was observed, and researchers describe this physical side effect as one of the main discriminants between NBOMe compounds and LSD. [16] [17] [18]

Neurotoxic and cardiotoxic actions

Many of the NBOMe compounds have high potency agonist activity at additional 5-HT receptors and prolonged activation of 5-HT2B can cause cardiac valvulopathy in high doses and chronic use. [3] [8] 5-HT2B receptors have been strongly implicated in causing drug-induced valvular heart disease. [19] [20] [21] The high affinity of NBOMe compounds for adrenergic α1 receptor has been reported to contribute to the stimulant-type cardiovascular effects. [8]

In vitro studies, 25C-NBOMe has been shown to exhibit cytotoxicity on neuronal cell lines SH-SY5Y, PC12, and SN471, and the compound was more potent than methamphetamine at reducing the visibility of the respective cells; the neurotoxicity of the compound involves activation of MAPK/ERK cascade and inhibition of Akt/PKB signaling pathway. [4] 25C-NBOMe, including the other derivative 25D-NBOMe, reduced the visibility of cardiomyocytes H9c2 cells, and both substances downregulated expression level of p21 (CDC24/RAC)-activated kinase 1 (PAK1), an enzyme with documented cardiac protective effects. [4]

Preliminary studies on 25C-NBOMe have shown that the substance is toxic to development, heart health, and brain health in zebrafish, rats, and Artemia salina , a common organism for studying potential drug effects on humans, but more research is needed on the topic, the dosages, and if the toxicology results apply to humans. Researchers of the study also recommended further investigation of the drug's potential in damaging pregnant women and their fetus due to the substance's damaging effects to development. [22] [23]

Emergency treatment

At present, there are no specific antidotes for NBOMes, and all acute intoxication is managed by symptomatic treatments, such as administration of benzodiazepines, antipsychotic drugs, and antiarrhythmic agents, such as beta blockers; some emergency interventions are intended to specifically treat rhabdomyolysis, which may lead to critical complications such as metabolic acidosis and acute kidney injury. [4]

Legality

United Kingdom

This substance is a Class A drug in the United Kingdom as a result of the N-benzylphenethylamine catch-all clause in the Misuse of Drugs Act 1971 . [24]

Notes

  1. The potency of N-benzylphenethylamines via buccal, sublingual, or nasal absorption is 50-100 greater (by weight) than oral route compared to the parent 2C-x compounds. [14] Researchers hypothesize the low oral metabolic stability of N-benzylphenethylamines is likely causing the low bioavailability on the oral route, although the metabolic profile of this compounds remains unpredictable; therefore researchers state that the fatalities linked to these substances may partly be explained by differences in the metabolism between individuals. [14]

Related Research Articles

<span class="mw-page-title-main">LSD</span> Hallucinogenic drug

Lysergic acid diethylamide, commonly known as LSD, is a potent psychedelic drug that intensifies thoughts, emotions, and sensory perception. Often referred to as acid or lucy, LSD can cause mystical, spiritual, or religious experiences. At higher doses, it primarily induces visual and auditory hallucinations. While LSD does not cause physical addiction, it can lead to adverse psychological reactions, such as anxiety, paranoia, and delusions. Additionally, it may trigger "flashbacks," also known as hallucinogen persisting perception disorder, where individuals experience persistent visual distortions after use.

<span class="mw-page-title-main">Serotonin receptor agonist</span> Neurotransmission-modulating substance

A serotonin receptor agonist is an agonist of one or more serotonin receptors. They activate serotonin receptors in a manner similar to that of serotonin, a neurotransmitter and hormone and the endogenous ligand of the serotonin receptors.

<span class="mw-page-title-main">25I-NBOH</span> Chemical compound

25I-NBOH is a derivative of the phenethylamine-derived hallucinogen 2C-I that was discovered in 2006 by a team at Purdue University.

<span class="mw-page-title-main">25I-NBOMe</span> Synthetic hallucinogen

25I-NBOMe, also known as Smiles, or N-Bomb, is a novel synthetic psychoactive substance with strong hallucinogenic properties, synthesized in 2003 for research purposes. Since 2010, it has circulated in the recreational drug scene, often misrepresented as LSD.

<span class="mw-page-title-main">25B-NBOMe</span> Chemical compound

25B-NBOMe is a derivative of the phenethylamine psychedelic 2C-B, discovered in 2004 by Ralf Heim at the Free University of Berlin. It acts as a potent full agonist for the 5HT2A receptor. Duration of effects lasts about 3–10 hours, although the parent compound is rapidly cleared from the blood when used in the radiolabeled form in tracer doses. Recently, Custodio et al. (2019) evaluated the potential involvement of dysregulated dopaminergic system, neuroadaptation, and brain wave changes which may contribute to the rewarding and reinforcing properties of 25B-NBOMe in rodents.

<span class="mw-page-title-main">25I-NBF</span> Chemical compound

25I-NBF is a derivative of the phenethylamine hallucinogen 2C-I, which acts as a highly potent partial agonist for the human 5-HT2A receptor, with bias towards the β-arrestin 2 coupled signalling pathway. It has been studied in its 11C radiolabelled form as a potential ligand for mapping the distribution of 5-HT2A receptors in the brain, using positron emission tomography (PET).

<span class="mw-page-title-main">25TFM-NBOMe</span> Chemical compound

25TFM-NBOMe is a derivative of the phenethylamine hallucinogen 2C-TFM, discovered in 2004 by Ralf Heim at the Free University of Berlin. It acts as a potent partial agonist for the 5-HT2A receptor, though its relative potency is disputed, with some studies finding it to be of lower potency than 25I-NBOMe, while others show it to be of similar or higher potency, possibly because of differences in the assay used. 2C-TFM-NB2OMe can be taken to produce psychedelic effects similar to 2C-I-NB2OMe and 2C-D-NB2OMe.

<span class="mw-page-title-main">25C-NBOMe</span> Psychedelic drug

25C-NBOMe is a psychedelic drug and derivative of the psychedelic phenethylamine 2C-C. 25C-NBOMe appeared on online vendor sites in 2010 but was not reported in the literature until 2011. It acts as a potent agonist of the 5-HT2A receptor, and has been studied in its 11C radiolabelled form as a potential ligand for mapping the distribution of 5-HT2A receptors in the brain, using positron emission tomography (PET). Multiple deaths have occurred from usage of 25C-NBOMe due to the ease of accidental overdose. The long-term toxic effects of the drug have not been researched.

<span class="mw-page-title-main">25D-NBOMe</span> Chemical compound

25D-NBOMe is a derivative of the phenethylamine derived hallucinogen 2C-D. It acts in a similar manner to related compounds such as 25I-NBOMe, which is a potent agonist at the 5-HT2A receptor. 25D-NBOMe has been sold as a street drug since 2010 and produces similar effects in humans to related compounds such as 25I-NBOMe and 25C-NBOMe. It was banned as a Temporary Class Drug in the UK on 10 June 2013 after concerns about its recreational use.

<span class="mw-page-title-main">25C-NBOH</span> Chemical compound

25-C-NBOH is a derivative of the phenethylamine derived hallucinogen 2C-C which has been sold as a designer drug. It has similar serotonin receptor affinity to the better-known compound 25C-NBOMe.

<span class="mw-page-title-main">25CN-NBOMe</span> Chemical compound

25CN-NBOMe is a derivative of the phenethylamine 2C-CN. It acts in a similar manner to related compounds such as 25I-NBOMe, which are potent agonists at the 5HT2A receptor.

<span class="mw-page-title-main">25N-NBOMe</span> Chemical compound

25N-NBOMe is a derivative of the hallucinogen 2C-N. The pharmacological properties of 25N-NBOMe have not been described in the scientific literature, but it is believed to act in a similar manner to related compounds such as 25I-NBOMe and 25C-NBOMe, which are potent agonists at the 5HT2A receptor. 25N-NBOMe has been sold as a street drug and has only been described in the literature in terms of identification by forensic analysis.

<span class="mw-page-title-main">25E-NBOMe</span> Chemical compound

25E-NBOMe is a derivative of the phenethylamine 2C-E. It acts in a similar manner to related compounds such as 25I-NBOMe, which are potent agonists at the 5-HT2A receptor. 25E-NBOMe has been sold as a drug and produces similar effects in humans to related compounds such as 25I-NBOMe and 25C-NBOMe.

<span class="mw-page-title-main">25P-NBOMe</span> Chemical compound

25P-NBOMe is a derivative of the phenethylamine 2C-P. It acts in a similar manner to related compounds such as 25I-NBOMe, which are potent agonists at the 5-HT2A receptor. 25P-NBOMe has been sold as a drug and produces similar effects in humans to related compounds such as 25I-NBOMe and 25C-NBOMe.

<span class="mw-page-title-main">25I-NB34MD</span> Derivative of the phenethylamine hallucinogen 2C-I

25I-NB34MD (NB34MD-2C-I) is a derivative of the phenethylamine hallucinogen 2C-I, which acts as a potent partial agonist for the human 5-HT2A receptor, and presumably has similar properties to 2C-I. It has a binding affinity of 0.67nM at the human 5-HT2A receptor, making it several times weaker than its positional isomer 25I-NBMD and a similar potency to 25I-NBF.

<span class="mw-page-title-main">25G-NBOMe</span> Chemical compound

25G-NBOMe (NBOMe-2C-G) is a derivative of the phenethylamine hallucinogen 2C-G, which acts as a highly potent agonist for the human 5-HT2A receptor.

<span class="mw-page-title-main">25H-NBOMe</span> Chemical compound

25H-NBOMe (NBOMe-2C-H) is a derivative of the phenethylamine hallucinogen 2C-H, which acts as a highly potent full agonist for the human 5-HT2A receptor.

<span class="mw-page-title-main">25-NB</span> Family of serotonergic psychedelics

The 25-NB (25x-NBx) series, sometimes alternatively referred to as the NBOMe compounds, is a family of serotonergic psychedelics. They are substituted phenethylamines and were derived from the 2C family. They act as selective agonists of the serotonin 5-HT2A receptor. The 25-NB family is unique relative to other classes of psychedelics in that they are, generally speaking, extremely potent and relatively selective for the 5-HT2A receptor. Use of NBOMe series drugs has caused many deaths and hospitalisations since the drugs popularisation in the 2010s. This is primarily due to their high potency, unpredictable pharmacokinetics, and sellers passing off the compounds in the series as LSD.

<span class="mw-page-title-main">25E-NBOH</span> Chemical compound

25E-NBOH is a derivative of the phenethylamine derived hallucinogen 2C-E. It was first developed by Martin Hansen at the University of Copenhagen in 2010 as a brain imaging agent, but has subsequently been sold as a designer drug, first being identified in Brazil in 2018 on seized blotter paper, as well as in Slovenia and France. It acts as a potent serotonin receptor agonist with similar affinity to better-known compounds such as 25I-NBOMe at 5-HT2A and 5-HT2C receptors.

<span class="mw-page-title-main">N-Benzyl-2C-B</span> Chemical compound

N-Benzyl-2C-B is a recreational designer drug from the 25-NB subgroup of the substituted phenethylamine family, with psychedelic effects. It has a binding affinity (Ki) of 16 nM at the serotonin receptor 5-HT2A and 90 nM at 5-HT2C and reportedly has a potency in between that of 2C-B and NBOMe-2C-B.

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